ABSTRACT
The quantitative relationship between glial fibrillary acidic protein (GFAP) hyper-reactivity and -amyloid protein (AP) deposition was investigated by double immunoperoxidase labeling of hippocampal and entorhinal cortex sections from five Alzheimer´s disease (AD) cases and five age-matched controls. AP plaques, which were absent in controls, were found in all AD samples, without significant differences in number or perimeter according to their location among the regions studied. In contrast, the mean number of GFAP (+) cells was significantly greater in the hippocampus than in the entorhinal cortex from AD cases (49 vs.39). Although at lower values (30 vs. 20), predominance of astrocyte hyperplasia in hippocampus as compared with entorhinal cortex was also found in control samples. Concomitant astrocyte hypertrophy, as defined by surface density (Sv) values of GFAP-immunoreactive material exceeding those of control means, affected a similar proportion of cells in the hippocampus (73%) and the entorhinal cortex (74%) from AD cases. Since an increased number of GFAP (+) cells in the hippocampus was not accompanied by an increased number and/or perimeter of neighbouring plaques, such differential hyper-reactivity in samples from AD patients, as well as in those with normal aging, seems to depend partially on the regional location of the involved astrocyte.
Subject(s)
Aged , Humans , Aging/pathology , Alzheimer Disease/pathology , Astrocytes/pathology , Amyloid beta-Peptides/analogs & derivatives , Astrocytes/cytology , Case-Control Studies , Cell Count , Entorhinal Cortex/chemistry , Entorhinal Cortex/pathology , Glial Fibrillary Acidic Protein/analysis , Hippocampus/chemistry , Hippocampus/pathology , ImmunohistochemistryABSTRACT
Lesions of the entorhinal cortex produce retrograde memory impairment in both animals and humans. Here we report the effects of bilateral entorhinal cortex lesions caused by the stereotaxic infusion of N-methyl-D-aspartate (NMDA) in rats at two different moments, before or after the training session, on memory of different tasks: two-way shuttle avoidance, inhibitory avoidance and habituation to an open field. Pre-or post-training entorhinal cortex lesions caused an impairment of performance in the shuttle avoidance task, which agrees with the previously described role of this area in the processing of memories acquired in sucessive sessions. In the inhibitory avoidance task, only the post-training lesions had an effect (amnesia). No effect was observed on the open field task. The findings suggest that the role of the entorhinal cortex in memory processing is task-dependent, perhaps related to the complexity of each task.